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Cocaine is a natural alkaloid derived from the leaves of Erythroxylum coca. Cocaine hydrochloride (powder cocaine) is a crystalline white powder. “Crack,” the free-base of cocaine hydrochloride, is an off-white substance named both for its rock-like appearance (“rock”) and due to the sound it makes when heated. In contrast to powder cocaine, crack may be smoked as it vaporizes instead of burning.
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Cocaine intoxication manifests as a sympathomimetic toxidrome, with tachycardia, hypertension, diaphoresis, mydriasis, delirium, and hyperthermia. Increased muscular activity may result in rhabdomyolysis. Numerous neurological complications have been reported after cocaine use, including subarachnoid hemorrhage, intracerebral hemorrhage, cerebral infarction, and seizures.
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Cardiovascular toxicity, including acute myocardial infarction, is well described after cocaine use. Dysrhythmias, including supraventricular tachycardia, atrial fibrillation and flutter, ventricular tachycardia, ventricular fibrillation, and torsades de pointes have been reported. Cocaine is a sodium channel blocker and may cause QRS widening on the electrocardiogram (ECG). Aortic dissection and rupture have been associated with cocaine use.
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Pulmonary effects of cocaine use include reactive airway disease exacerbation, pneumothorax, pneumomediastinum, and cardiogenic and noncardiogenic pulmonary edema (NCPE). “Crack-lung” refers to an acute pulmonary syndrome of dyspnea, hypoxia, and diffuse pulmonary alveolar infiltrates.
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Management and Disposition
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Treatment is primarily supportive, and focuses upon the signs and symptoms of toxicity. No specific antidote exists. Cardiac monitoring is indicated for symptomatic patients. Initial management focuses upon control of agitation and hyperthermia, and prevention of complications (eg, rhabdomyolysis). The use of neuroleptic agents is relatively contraindicated for cocaine-associated psychomotor agitation due to the negative effects of these agents on thermoregulation, seizure threshold, and the potential for dysrhythmias. Benzodiazepines are the first line of therapy for agitation. They also appear beneficial in the management of cocaine-associated chest pain. Sodium bicarbonate administration should be considered for QRS widening in the setting of acute cocaine poisoning.
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The use of β-blockers is contraindicated in the management of cocaine-associated chest pain and myocardial ischemia due to the potential for vasospasm and hypertensive crisis (“unopposed α-effect”).
Although the risk of myocardial infarction is greatest immediately after use, myocardial ischemia may occur up to 6 weeks after last use.
Cocaethylene may form in vivo after the use of cocaine and ethanol. Cocaethylene is more cardiotoxic than cocaine and has a longer half-life.
The rupture of a cocaine packet in a body-packer may result in fatal toxicity. Emergent surgical intervention may be considered for immediate removal of the packets.
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